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| Author(s): |
Gustavo Ligeri Pereira do Prado
Total Authors: 1
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| Document type: | Master's Dissertation |
| Press: | Campinas, SP. |
| Institution: | Universidade Estadual de Campinas (UNICAMP). Faculdade de Ciências Médicas |
| Defense date: | 2008-07-25 |
| Examining board members: |
Konradin Metze;
Jose Francisco Figueiredo;
Licio Augusto Velloso
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| Advisor: | Jose Antonio Rocha Gontijo; Konradin Metze |
| Abstract | |
Lead (Pb) is one of the most important naturally occurring and ubiquitous heavy metals, with toxic effects after acute or chronic exposure on liver, the nervous system, hematopoesis, and, especially the kidneys. The aim was to study the time course of the renal tubular sodium handling during chronic experimental lead poisoning in rats comparing it with the morphologic changes of epithelial cells of the proximal tubule. Male Wistar-Hannover rats were chronically intoxicated with daily i.p. injections of 2.5 ml/kg of 1% lead acetate solution and sacrificed after 8, 15, 30, 45 and 60 days. Kidney samples were examined by light and electron microscopy and by computerized texture analysis. Renal clearance as well as fractional proximal and postproximal renal sodium handling was studied. Sodium reabsorption at the proximal tubule decreased significantly after one week but recovered after one month and achieved a higher level than in controls until the end of the experiment. Ultrastuctural examinations showed mitochondrial swelling with degeneration and loss of microvilli but no striking alterations of the epithelial cell nuclei in the first two weeks. Karyometry revealed an increase in nuclear size during the experiment. The chromatin texture changed significantly between the 15th and 30th day concomitantly with the appearance of inclusion bodies. Energy values derived from Fast-Fourier-transformed images were more efficient in detecting differences between the groups than variables derived from the gray value co-occurrence matrix. Significant nuclear alterations occur between 15 and 30 days of chronic lead intoxication, paralleled by a normalization of the physiological renal ion reabsorption capacity. The formation of inclusion bodies, mitochondrial regeneration as well as an increased production of antioxidant proteins may be involved in this compensatory mechanism (AU) | |